1. Field of Invention
The present invention relates generally to the field of health. More particularly, the present invention relates to the use of a natural, strontium-based blend of ingredients to control the progression of osteoarthritis, osteoporosis, and tooth decay.
2. Description of Related Art
Osteoarthritis is the most common worldwide joint condition with symptomatic disease affecting up to 20% of individuals aged over 50 years. Moreover, the socioeconomic burden is immense, costing society hundreds of billions of dollars a year. The etiology of osteoarthritis is multi-factorial and may be due in part to gravitation effects on weight-bearing joints and result from repetitive, life-long, joint specific minor or more defined major injuries. Osteoarthritis frequently affects axial areas such as the neck or low back joints as well as appendicular small hand joints and weight-bearing joints such as the hip or knee or foot. Obesity appears to play a role at least in the progression of symptomatic osteoarthritis in weight-bearing joints by excessive loading on the involved joint.
Medical treatment of osteoarthritis is limited to pain and anti-inflammation medication usage coupled with joint specific targeted steroid or hyaluronic acid derivative injection therapy. Surgical joint replacement has improved and in general is reserved for end-stage symptomatic disease in individuals who are otherwise in good health and have exhausted nonsurgical alternatives. More recently, medical treatment emphasis has shifted to earlier diagnosis (via magnetic resonance imaging) and earlier pharmaceutical intervention. Despite this important insightful change, no pharmaceutical agent is currently available that can (1) treat pain while (2) preventing or slowing down disease progression.
From a biomechanical and microscopic viewpoint, osteoarthritis is characterized as a dynamic process of ongoing hyaline or fibrocartilage cartilage (e.g. knee meniscus) deterioration coupled with progressive adaptive subchondral bone remodeling. There is increasing evidence that this is indeed a coupled metabolic interaction between bone cells such as osteoblasts, osteocytes and osteoclasts and cartilage cells such as apoptotic (dying) chondrocytes and chondroblasts that is regulated in part by surrounding intercellular chemical signal and inflammatory factors. The key is that clinically this interplay results is painful joint dysfunction. The coupling of bone and cartilage turnover and ongoing cartilage degeneration has sparked interest in employing bone antiresorptive and anabolic agents as therapeutic drugs. Several investigations have shown a positive effect on cartilage when bone resorption is suppressed or progression of cartilage degradation when bone resorption is increased.
From a practical point of view, osteoporosis is best characterized by decreased bone mass coupled with increased risk of low impact fracture. The risk of osteoporosis increases with age. Worldwide, approximately 15% of the elderly (both men and women) are affected by this weakened bone condition which results in almost 9 million bone fractures (e.g., wrist, rib, vertebral, hip) every year. The mechanism of osteoporosis is a dysregulation of bone resorption and bone formation during ongoing bone remodeling. A combination of inadequate bone mass coupled with excessive bone resorption and suboptimal new bone formation during remodeling results in fragile bone tissue. An interplay of hormone deficiency (e.g., estrogen or testosterone), decreased vitamin d and deficiency of calcium can lead to increased bone resorption and poor new bone formation. At a cellular level, dysregulation of bone building osteoblasts and bone resorbing osteoclasts influenced by other extracellular inflammatory mediators play a significant role and underlie the development and progression of osteoporosis. Certain medications such as long-term use of glucocorticoids, anti-seizure medications, anticoagulants and proton pump inhibitors have a been linked to both the development or worsening of osteoporosis.
Treatment and prevention of osteoporotic weakened bone are aimed at maintaining adequate or restoring essential calcium and vitamin D bone stores. Usually, oral supplementation of these nutrients is coupled with weight bearing and muscle strengthening exercise. In addition, lifestyle changes that help include cessation of cigarette smoking and alcohol use. Pharmaceutical medications such as bisphosphonates or other anti-osteoporotic drugs such as denosumab which increase bone mineral density can also be employed. Bisphosphonates inhibit osteoclastic bone resorption by attaching to binding sites on bony surfaces while denosumab inhibits this maturation of osteoclasts. Direct stimulation of bone formation with parathyroid hormone related anabolic agents can also be employed. Use of these prescription medications are limited by cost, side effects and patient preference. Severe bisphosphonate adverse effects include bisphosphonate-related osteonecrosis of the jaw and atypical femur bone fractures. In the elderly, this can result in the loss of teeth, inability to undergo dental implant surgery and femur fracture repair.
Dental caries (tooth decay) remains a world-wide endemic problem and is the most common endemic dental issue in many populations. Dietary overuse of refined sugars such as sucrose are a well-established contributor to the increased rate of dental caries in developed societies. Tooth decay results from ongoing tooth surface caries formation over time. Ongoing deepening tooth decay frequently results in periodontal tooth infection and pain ultimately coupled with chewing failure and tooth loss. The tooth cavity starts at the tooth surface which consists of enamel or dentin. The involved tooth becomes surrounded by caries-causing bacteria which ferment carbohydrates such as sucrose or fructose. As part of this fermentation process, acids such as lactic acid are produced and accumulate around portions of tooth structure. In a susceptible host, these acids will cause tooth demineralization if left unchecked by the natural wetting, diluting and neutralizing action of saliva.
Oral use of xylitol, a natural sugar alcohol sweetener either in chewing gum or lozenge form, helps to prevent caries development since it is not fermentable in the oral cavity. In addition, xylitol can carry polyvalent cations like calcium or strontium into an arranged xylitol ligand for transport and presentation to the gut wall mucosa for improved systemic absorption. Possibly, this can help remineralize deeper enamel before further caries progression can develop. Fluoride containing toothpastes, although unnatural, are helpful by decreasing demineralization, in part by binding to the hydroxyapatite crystals in enamel.
Osteoarthritis, osteoporosis, and dental caries are not conditions that overlap in medical or scientific disciplines. For example, rheumatologists that specialize in joint conditions, orthopedists that specialize in bone and joint surgery, endocrinologists who specialize in bone metabolism disorders, and doctors of medical dentistry (DMDs) do not typically read one another's specific scientific research. As a result, there lacks a medical or scientific solution that mutually addresses these various conditions.
Based on the foregoing, there is a need in the art for a single solution that can control progression of and medically treat the three distinct disorders of osteoarthritis, osteoporosis, and dental caries (tooth decay).
The above problems in the related art are considered as matters that have been addressed by the inventor to derive the present inventive concept, or as matters discovered during the course of deriving the present inventive concept. Thus, the problems may not be simply referred to as information that was known to the general public prior to filing the present disclosure.